Histone Deacetylase 11 Contributes to Renal Fibrosis by Repressing KLF15 Transcription.

ABSTRACT: Renal fibrosis represents a key pathophysiological process in patients with chronic kidney diseases (CKD) and is typically associated with a poor prognosis. Renal tubular epithelial cells (RTECs), in response to a host of pro-fibrogenic stimuli, can trans-differentiate into myofibroblast-like cells and produce extracellular matrix proteins to promote renal fibrosis. In the present study we investigated the role of histone deacetylase 11 (HDAC11) in this process and the underlying mechanism. We report that expression levels of HDAC11 were up-regulated in the kidneys in several different animal models of renal fibrosis. HDAC11 was also up-regulated by treatment of Angiotensin II (Ang II) in cultured RTECs. Consistently, pharmaceutical inhibition with a small-molecule inhibitor of HDAC11 (qui

SUBMITTER: Mao L 

PROVIDER: S-EPMC7180197 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature